{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/112977"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/112977","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Aquaporin-4 mediates blood brain barrier permeability during endotoxemia","abstract":"Aquaporin-4 (AQP4) is a water channel expressed on astrocytes known to regulate the exchange of fluids and solutes between the parenchyma of the central nervous system (CNS) and perivascular spaces. We hypothesized that activation of AQP4 may mediate permeability of the CNS during systemic inflammation. Here, mice were i.v. injected with fluorescent tracers of low (1 kd) and intermediate (10 kd) molecular weights 24 hours after induction of endotoxemia with i.p. LPS. Fluorescent microscopy using tissue sections and cleared half-brains showed that endotoxemia increased tracer penetrance into the brain parenchyma. Temporal and spatial distribution of tracers suggested that penetrance occurred across neurovasculature, choroid plexus, and circumventricular organs (CVOs). Treatment with the AQP4 inhibitor, AER-271, blocked tracer passage across the glia limitans and caused tracer accumulation within perivascular spaces. These data show that AQP4 mediates the flux of solutes from the perivascular space to the brain parenchyma during systemic inflammation and highlight a novel strategy to neuroprotection during sepsis.","abstract_html":"Aquaporin-4 (AQP4) is a water channel expressed on astrocytes known to regulate the exchange of fluids and solutes between the parenchyma of the central nervous system (CNS) and perivascular spaces. We hypothesized that activation of AQP4 may mediate permeability of the CNS during systemic inflammation. Here, mice were i.v. injected with fluorescent tracers of low (1 kd) and intermediate (10 kd) molecular weights 24 hours after induction of endotoxemia with i.p. LPS. Fluorescent microscopy using tissue sections and cleared half-brains showed that endotoxemia increased tracer penetrance into the brain parenchyma. Temporal and spatial distribution of tracers suggested that penetrance occurred across neurovasculature, choroid plexus, and circumventricular organs (CVOs). Treatment with the AQP4 inhibitor, AER-271, blocked tracer passage across the glia limitans and caused tracer accumulation within perivascular spaces. These data show that AQP4 mediates the flux of solutes from the perivascular space to the brain parenchyma during systemic inflammation and highlight a novel strategy to neuroprotection during sepsis.","abstract_has_math":false,"creators":["Gonzalez Ricon, Rafael Jaime"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"M.S.","degree_level":"Thesis","degree_discipline":"Animal Sciences","degree_department":null,"school":null,"contributors":["McKim, Daniel Boyce","Rhodes, Justin","Raetzman, Lori"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2022,"date_issued":"2022-01-12T21:45:23Z","date_published":"2022-01-12T21:45:23Z","updated_at":"2026-07-22T22:24:52Z","subjects":["AQP4","Sepsis","Blood brain barrier (BBB)."],"languages":["en"],"rights":["Copyright 2021 Rafael Jaime Gonzalez Ricon"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/2142/112977","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["McKim, Daniel Boyce","Rhodes, Justin","Raetzman, Lori"]},{"key":"dc:creator","label":"Author","values":["Gonzalez Ricon, Rafael Jaime"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2022-01-12T21:45:23Z","2021-07-01","2021-08"]},{"key":"dc:type","label":"Dc Type","values":["text","Thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Animal Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["M.S."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["AQP4","Sepsis","Blood brain barrier (BBB)."]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 2021 Rafael Jaime Gonzalez Ricon"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/112977"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Aquaporin-4 (AQP4) is a water channel expressed on astrocytes known to regulate the exchange of fluids and solutes between the parenchyma of the central nervous system (CNS) and perivascular spaces. We hypothesized that activation of AQP4 may mediate permeability of the CNS during systemic inflammation. Here, mice were i.v. injected with fluorescent tracers of low (1 kd) and intermediate (10 kd) molecular weights 24 hours after induction of endotoxemia with i.p. LPS. Fluorescent microscopy using tissue sections and cleared half-brains showed that endotoxemia increased tracer penetrance into the brain parenchyma. Temporal and spatial distribution of tracers suggested that penetrance occurred across neurovasculature, choroid plexus, and circumventricular organs (CVOs). Treatment with the AQP4 inhibitor, AER-271, blocked tracer passage across the glia limitans and caused tracer accumulation within perivascular spaces. These data show that AQP4 mediates the flux of solutes from the perivascular space to the brain parenchyma during systemic inflammation and highlight a novel strategy to neuroprotection during sepsis.","Submission original under an indefinite embargo labeled 'Open Access'. The submission was exported from vireo on 2022-01-12 without embargo terms","The student, Rafael Jaime Gonzalez Ricon, accepted the attached license on 2021-06-28 at 16:24.","The student, Rafael Jaime Gonzalez Ricon, submitted this Thesis for approval on 2021-06-28 at 16:46.","This Thesis was approved for publication on 2021-07-01 at 11:46.","DSpace SAF Submission Ingestion Package generated from Vireo submission #16727 on 2022-01-12 at 12:43:39","Made available in DSpace on 2022-01-12T21:45:23Z (GMT). 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Here, mice were i.v. injected with fluorescent tracers of low (1 kd) and intermediate (10 kd) molecular weights 24 hours after induction of endotoxemia with i.p. LPS. Fluorescent microscopy using tissue sections and cleared half-brains showed that endotoxemia increased tracer penetrance into the brain parenchyma. Temporal and spatial distribution of tracers suggested that penetrance occurred across neurovasculature, choroid plexus, and circumventricular organs (CVOs). Treatment with the AQP4 inhibitor, AER-271, blocked tracer passage across the glia limitans and caused tracer accumulation within perivascular spaces. These data show that AQP4 mediates the flux of solutes from the perivascular space to the brain parenchyma during systemic inflammation and highlight a novel strategy to neuroprotection during sepsis.","Submission original under an indefinite embargo labeled 'Open Access'. The submission was exported from vireo on 2022-01-12 without embargo terms","The student, Rafael Jaime Gonzalez Ricon, accepted the attached license on 2021-06-28 at 16:24.","The student, Rafael Jaime Gonzalez Ricon, submitted this Thesis for approval on 2021-06-28 at 16:46.","This Thesis was approved for publication on 2021-07-01 at 11:46.","DSpace SAF Submission Ingestion Package generated from Vireo submission #16727 on 2022-01-12 at 12:43:39","Made available in DSpace on 2022-01-12T21:45:23Z (GMT). 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